CELL-MATRIX ADHESIONS AND LOCALIZATION OF THE VITRONECTIN RECEPTOR INMCF-7 HUMAN MAMMARY-CARCINOMA CELLS

Interference reflection microscopy (IRM) was used to evaluate the stat us of cell matrix adhesions in the MCF-7 human mammary carcinoma cell line. Focal contacts were concentrated at the periphery of individual cells or small cell clusters. Close contact was detected as a band at cell peripheries and as localized patches throughout the ventral face of cells. The MCF-7 cells also exhibited a distinctive reflection patt ern of an intensity midway between that of either focal or close conta ct. This novel reflection pattern was located primarily at the periphe ry of cells and often obscured visualization of focal contacts in live cells. A similar distinctive pattern was absent from the normal tissu e-derived MCF-10A mammary epithelial cell line. Immunofluorescence sta ining using an antiserum that cross-reacts with both alpha(v)beta(3) a nd alpha(v)beta(5) integrins revealed a distribution of the vitronecti n receptor similar to that of the novel adhesion pattern as well as to that of focal contacts. In addition, IRM demonstrated the presence of ''tracks'' associated with cells, which were also stained with the vi tronectin receptor antiserum. The tracks are apparently residual mater ial left behind as a result of cell migration. When MCF-7 cells were c ultured in the absence of estradiol, the tracks were greatly diminishe d when visualized with either IRM or staining for the vitronectin rece ptor. In contrast, the addition of l7-beta-estradiol to the medium res ulted in an increased presence of the tracks as well as the developmen t of extensive close contacts throughout the ventral surface of cells and cell clusters. Cells treated with the estrogen antagonist ICI 182, 720 in the presence of estradiol had few associated tracks, indicating that the process leading to the formation of these structures is depe ndent on an estrogen receptor-activated pathway. However, the antagoni st did not prevent the estradiol-induced formation of extensive close contacts. The extensive close contact as well as the increase in trail ing material suggests that estradiol may promote breast tumor cell :mo tility. However, this migratory activity may be mediated by both estro gen receptor-dependent and -independent pathways.